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BackgroundThe aim of our study was to investigate and control an outbreak and identify risk factors for colonization and infection with Serratia marcescens in two departments in Tartu University Hospital.MethodsThe retrospective case–control study was conducted from July 2005 to December 2006. Molecular typing by pulsed field gel electrophoresis was used to confirm the relatedness of Serratia marcescens strains. Samples from the environment and from the hands of personnel were cultured.ResultsThe outbreak involved 210 patients, 61 (29%) developed an infection, among them 16 were invasive infections. Multivariate analysis identified gestational age, arterial catheter use and antibiotic treatment as independent risk factors for colonization and infection with Serratia marcescens. Molecular typing was performed on 83 Serratia marcescens strains, 81 of them were identical and 2 strains were different.ConclusionsGiven the occasionally severe consequences of Serratia marcescens in infants, early implementation of aggressive infection control measures involving patients and mothers as well as the personnel is of utmost importance.

The aim of this study was to analyze all deaths from A (H1N1) in Estonia during the 2009–2010 epidemic to find out the reasons of high mortality and optimize management strategies for future influenza epidemics. Material and Methods. A retrospective review of medical records, autopsy reports, and reassessment of autopsy slides of all fatal cases of proven A (H1N1) influenza in Estonia from October 2009 to May 2010 was carried out. Results. There were a total of 21 proven fatal cases (median age, 57 years); the population mortality rate of 1.56 per 100 000 inhabitants was one of the highest in the world. Altogether, 18 of the 21 patients had known risk factors for influenza, and 3 patients were previously healthy children. Three decedents had received antiviral treatment, and none had been immunized. There were 19 decedents autopsied, with viral pneumonia (58%) being the most frequent pathological finding; 40% had evidence of bacterial superinfection. In 4 cases, influenza was not clinically suspected and was diagnosed postmortem. Influenza was the primary cause of death in 15 decedents, while in 9 cases, comorbidities played a significant role in fatal outcome. In the remaining 4 cases, another illness was considered the primary cause of death with influenza as an accompanying factor. Conclusions. High autopsy rate and liberal postmortem PCR testing enables the detection of additional A (H1N1) influenza cases, yet it might lead to overestimation of the population mortality rates, especially in a small population with low number of events. Increased vaccine coverage, vigilant diagnosing including wide PCR testing, and early more liberal use of antiviral medications during the influenza A (H1N1) epidemic may hold the potential of lowering population mortality.

This prospective cohort study was performed from April to December 2003 for the purpose of collecting a maximum of 50 non-duplicate isolates of Acinetobacter baumannii, Pseudomonas aeruginosa, and Klebsiella pneumoniae from each of 4 ICUs to determine minimum inhibitory concentrations. The most prevalent species were Enterobacteriaceae (13%), K. pneumoniae and A. baumannii (both 12%). 60% of A. baumannii strains were susceptible to ampicillin/sulbactam and cefepime, 95% to meropenem and imipenem, and 75% to amikacin. 79% of P. aeruginosa strains were piperacillin/tazobactam, 58% ceftazidime, 81% meropenem, 72% imipenem, 69% ciprofloxacin and 97% amikacin susceptible. The susceptibility of K. pneumoniae to meropenem and imipenem was 99%, to ciprofloxacin was 91% and to amikacin was 98%. Gram-negative bacteria (especially K. pneumoniae and A. baumannii) were prevalent in our ICUs compared to other European studies. Carbapenem susceptibility of Estonian strains was higher, but P. aeruginosa sensitivity to ceftazidime was lower, compared to other EU countries.